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PM2.5 and its main chemical components have been investigated during six air pollution periods across four seasons from Jun. 16, 2016 to Jun. 15, 2017 at a suburban site in Beijing, China. Daily PM2.5 mass concentrations were measured with associated ions, OC, EC, 16 PAHs and seven heavy metals. Mass closure analyses were conducted using measured and reconstructed chemical components. Chemical ratios were used to identify possible pollution sources, while principal component analysis (PCA) coupled with multiple linear regression (MLR) method was used to estimate the source contribution to PM2.5 mass. The annual mean PM2.5 concentration (96.7 μg m−3) is about 2.8 times the national level-2 standard limit, with apparent seasonal variation of daily exceedances as winter > spring > autumn > summer. Generally, higher levels are observed in winter and autumn than in spring and summer for NO3−, SO42−, NH4+, Cl−, K+, OC, EC, PAHs and metals Zn, As, Cu, Pb, along with higher concentrations of NOx, CO and SO2. Secondary ions and carbon fractions are most abundant over all seasons, except levels of dust related species Ca2+, Mg2+, Ca, Fe and Mn are also high in spring. The reconstructed results show that PM2.5 consists of mostly organic compounds (26–38%) and ammonium salts (NH4NO3 + (NH4)2SO4) (43–53%) in winter and autumn, while summer is dominated mainly by ammonium salts (81%). In spring, very high PM2.5 episodes are occasionally composed of large amount of soil/road dust and gypsum particles (23–55%) due to floating dust events with drier weather conditions and human activities. Fuel combustions and secondary sources are responsible for ~70% of PM2.5 mass while mobile source is mostly a regional origin.

Abnormally expressed long non-coding RNAs (lncRNAs) have been recognized as potential diagnostic biomarkers or therapeutic targets in non-small cell lung cancer (NSCLC). The role of the novel lnc-CYB561-5 in NSCLC and its specific biological activity remain unknown. In this study, lncRNAs highly expressed in NSCLC tissue samples compared with paired adjacent normal tissue samples and atypical adenomatous hyperplasia were identified by RNA-seq analysis. Lnc-CYB561-5 is highly expressed in human NSCLC and is associated with a poor prognosis in lung adenocarcinoma. In vivo, downregulation of lnc-CYB561-5 significantly decreases tumour growth and metastasis. In vitro, lnc-CYB561-5 knockdown treatment inhibits cell migration, invasion and proliferation ability, as well as glycolysis rates. In addition, RNA pulldown and RNA immunoprecipitation (RIP) assays show that basigin (Bsg) protein interacts with lnc-CYB561-5. Overall, this study demonstrates that lnc-CYB561-5 is an oncogene in NSCLC, which is involved in the regulation of cell proliferation and metastasis. Lnc-CYB561-5 interacts with Bsg to promote the expression of Hk2 and Pfk1 and further lead to metabolic reprogramming of NSCLC cells.

Objective Guanylate‐binding protein 1 (GBP1) is reported to promote tumor progression and treatment resistance in lung cancer, and presents as a prognostic biomarker in several solid tumors. However, the related research of GBP1 in clinical management of lung adenocarcinoma is still lacking. Therefore, the present study aimed to detect the clinical role of GBP1 in lung adenocarcinoma. Methods The clinical data of 221 lung adenocarcinoma patients were retrospectively analyzed, and then, their tumor tissue specimens and paired adjacent tissue specimens were retrieved for GBP1 detection via immunohistochemistry (IHC) assay. Results GBP1 expression was upregulated in tumor tissues compared with adjacent tissues (P, Objective: Guanylate‐binding protein 1 (GBP1) is reported to promote tumor progression and treatment resistance in lung cancer, and presents as a prognostic biomarker in several solid tumors. However, the related research of GBP1 in clinical management of lung adenocarcinoma is still lacking. Therefore, the present study aimed to detect the clinical role of GBP1 in lung adenocarcinoma. Methods: The clinical data of 221 lung adenocarcinoma patients were retrospectively analyzed, and then, their tumor tissue specimens and paired adjacent tissue specimens were retrieved for GBP1 detection via immunohistochemistry (IHC) assay. According to total GBP1 IHC stain scoring in specimens, the score ≤3 was defined as GBP1 low expression, while the score >3 was defined as GBP1 high expression. Results: GBP1 expression was upregulated in tumor tissues compared with adjacent tissues (P

The developmental pluripotency-associated 4 (Dppa4) gene serves critical roles in cell self-renewal, as well as in cancer development and progression. However, the regulatory role of Dppa4 in non-small-cell lung cancer (NSCLC) and its underlying mechanisms remain elusive. The aim of the present study was to investigate the biological function of Dppa4 in NSCLC and its underlying mechanism of action. Dppa4 expression was measured in NSCLC tissue samples and cell lines, and its effect on cell proliferation and the expression of glycolytic enzymes was determined. In addition, the underlying mechanisms of Dppa4-induced alterations in glycolysis were analyzed. Univariate and multivariate analyses were also performed to analyze the prognostic significance of clinicopathological characteristics. Dppa4 was found to be highly expressed in NSCLC tissues and cell lines. Furthermore, it was observed that Dppa4 was correlated with the degree of tumor differentiation and TNM stage. Univariate and multivariate analyses identified Dppa4 expression and clinical stage as prognostic factors for NSCLC patients. Kaplan-Meier analysis further revealed that patients with lower Dppa4 expression exhibited a better prognosis. In NSCLC cells, Dppa4 knockdown inhibited cell proliferation, while Dppa4 overexpression enhanced cell proliferation, which was likely mediated by glycolysis promotion. Dppa4 knockdown had no evident effect on the majority of enzymes examined; however, glucose transporter type 4 (GLUT-4) and pyruvate kinase isozyme M2 were significantly upregulated, and hexokinase II (HK-II) and lactate dehydrogenase B (LDHB) were downregulated following Dppa4 knockdown. By contrast, Dppa4 overexpression resulted in downregulation of GLUT-4, and upregulation of HK-II, enolase and LDHB, whereas it had no effect on other enzymes. Since the most evident effect was observed on LDHB, further functional experiments demonstrated that this enzyme reversed the promoting effects of Dppa4 in NSCLC. In conclusion, Dppa4 promotes NSCLC progression, partly through glycolysis by LDHB. Thus, the Dppa4-LDHB axis critically contributes to glycolysis in NSCLC cells, thereby promoting NSCLC development and progression.

The research object of this study is “ML7113” wheat leaf, which is used to isolate protoplast with enzyme hydrolysis method. Three main effectors—the concentration of mannitol, enzymolysis time and centrifugal force, affect the production and vitality of protoplast. While the production and vitality of wheat protoplasts were detected by the hemacytometer and the FDA staining respectively. Results showed that, with the increasing concentrations of mannitol during 0.2 M - 0.4 M, protoplast yield increases and when the concentration is 0.4 M, the protoplast vitality can be up to 95%; with the extension of enzymolysis time in 2 h to 8 h, protoplast yield reaches a maximum in 6 h, but its vitality achieves the maximum in 4 h; considering a combination of these two factors impacting on protoplast, we obtain the best time to digest for 4 h; meanwhile, with the increasing of the centrifugal force from 500 rpm - 2000 rpm, its comprehensive effect of protoplast vitality and yield is the highest when the centrifugal force is 1000 rpm for 2 min (replicated three times). So 0.4 M mannitol, 4 h enzymolysis time and 1000 rpm for 2 min centrifugal force are the best separation condition.

Family cooking oil fume are becoming an important source of urban atmospheric fine particulate (PM2.5). In order to understand the characteristics and level of PM2.5 emission from family cooking fume. Mass concentration, chemical compositions and emission factors of PM2.5 emitted from family cooking fumes were studied based on in situ measurement, and the total amounts of PM2.5 emission from family cooking fumes in Beijing was preliminary estimated. Results showed that mass concentration of PM2.5 emitted from family cooking fumes ranged from 329.88±91.24 to 500.89±130.44 μg·m−3, the average mass concentration was 398.82±102.55 μg·m−3. Among all the measured chemical components of organic carbon (OC), water-soluble ions and element carbon (EC) account for about 51.34%-65.45%, 6.93%-14.78% and 0.73%-1.82%, respectively, other untested components account for about 19.44%-38.05%. According to the field investigation and actual measurement, the average PM2.5 emission factor was 210.57±54.15 mg·f·d−1 based on household number. Combined with the 2018 statistics annual report of Beijing, the total amounts of PM2.5 emission from family cooking oil fumes in Beijing was estimated to be 553.38±142.31 t·a−1 in 2018. The emission amounts has certain uncertainty, the following work should be carried out to measure the PM2.5 emission from family cooking oil fumes in different administrative regions.